Allen L. Alcivar
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View article: Table S2 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Table S2 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Single nucleotide polymorphisms (SNP) in Capan1 olaparib resistant cells
View article: Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Patients harboring germline breast cancer susceptibility genes 1 and 2 (BRCA1/2) mutations are predisposed to developing breast, pancreatic, and ovarian cancers. BRCA2 plays a critical role in homologous recombination (HR) DNA repair and d…
View article: Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Patients harboring germline breast cancer susceptibility genes 1 and 2 (BRCA1/2) mutations are predisposed to developing breast, pancreatic, and ovarian cancers. BRCA2 plays a critical role in homologous recombination (HR) DNA repair and d…
View article: Supplementary Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Supplementary Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Supplementary methods and figure legends. Figure S1 shows further characterization of Capan1 olaparib resistant cells and rucaparib resistant Capan1 cells. Figure S2 shows that drug efflux is unchanged in Capan1 olaparib resistant cells an…
View article: Table S1 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Table S1 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Gene Expression of Capan1 olaparib resistant cells
View article: Table S3 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Table S3 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Immunoprecipitation of BRCA2 . List of proteins identified via mass spectrometry.
View article: Table S2 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Table S2 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Single nucleotide polymorphisms (SNP) in Capan1 olaparib resistant cells
View article: Supplementary Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Supplementary Data from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Supplementary methods and figure legends. Figure S1 shows further characterization of Capan1 olaparib resistant cells and rucaparib resistant Capan1 cells. Figure S2 shows that drug efflux is unchanged in Capan1 olaparib resistant cells an…
View article: Table S3 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Table S3 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Immunoprecipitation of BRCA2 . List of proteins identified via mass spectrometry.
View article: Table S1 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Table S1 from Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Gene Expression of Capan1 olaparib resistant cells
View article: Supplementary Figure 3 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 3 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
High DPP3 mRNA expression correlates with poor relapse-free survival (RFS) of breast cancer patients in the Kaplan-Meier Plotter database.
View article: Data from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Data from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
NRF2 is a transcription factor serving as a master regulator of the expression of many genes involved in cellular responses to oxidative and other stresses. In the absence of stress, NRF2 is constantly synthesized but maintained at low lev…
View article: Supplementary Figure 5 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 5 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Effect of mutating individual cysteine residues of DPP3 on its interaction with KEAP1.
View article: Data from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Data from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
NRF2 is a transcription factor serving as a master regulator of the expression of many genes involved in cellular responses to oxidative and other stresses. In the absence of stress, NRF2 is constantly synthesized but maintained at low lev…
View article: Supplementary Figure 4 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 4 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Effect of mutating individual cysteine residues of KEAP1 on DPP3 binding.
View article: Supplementary Figure 4 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 4 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Effect of mutating individual cysteine residues of KEAP1 on DPP3 binding.
View article: Supplementary Figure 1 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 1 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Effect of N-acetylcystein (NAC) on the DPP3-KEAP1 interaction.
View article: Supplementary Figure 2 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 2 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
mRNA levels of DPP3, NRF2, NQO1, GCLM, KEAP1 and p62 in MCF7 cell lines stably overexpressing wt and mutant DPP3 species.
View article: Supplementary Figure 5 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 5 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Effect of mutating individual cysteine residues of DPP3 on its interaction with KEAP1.
View article: Supplementary Figure 2 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 2 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
mRNA levels of DPP3, NRF2, NQO1, GCLM, KEAP1 and p62 in MCF7 cell lines stably overexpressing wt and mutant DPP3 species.
View article: Supplementary Figure 1 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 1 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Effect of N-acetylcystein (NAC) on the DPP3-KEAP1 interaction.
View article: Supplementary Material and Methods from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Material and Methods from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Quantification of mRNA amount, qRT-PCR primer sequences, and transfection and immunoprecipitation methods.
View article: Supplementary Figure 3 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Figure 3 from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
High DPP3 mRNA expression correlates with poor relapse-free survival (RFS) of breast cancer patients in the Kaplan-Meier Plotter database.
View article: Supplementary Material and Methods from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
Supplementary Material and Methods from NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
Quantification of mRNA amount, qRT-PCR primer sequences, and transfection and immunoprecipitation methods.
View article: BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage
BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage Open
The BRCA2 tumor suppressor protects genome integrity by promoting homologous recombination-based repair of DNA breaks, stability of stalled DNA replication forks and DNA damage-induced cell cycle checkpoints. BRCA2 deficient cells display …
View article: Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations
Amplification of the Mutation-Carrying BRCA2 Allele Promotes RAD51 Loading and PARP Inhibitor Resistance in the Absence of Reversion Mutations Open
Patients harboring germline breast cancer susceptibility genes 1 and 2 (BRCA1/2) mutations are predisposed to developing breast, pancreatic, and ovarian cancers. BRCA2 plays a critical role in homologous recombination (HR) DNA repair and d…
View article: NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction
NRF2 Induction Supporting Breast Cancer Cell Survival Is Enabled by Oxidative Stress–Induced DPP3–KEAP1 Interaction Open
NRF2 is a transcription factor serving as a master regulator of the expression of many genes involved in cellular responses to oxidative and other stresses. In the absence of stress, NRF2 is constantly synthesized but maintained at low lev…